Posterior Fossa Acute Extradural Hematoma in Children: Review and Management Guidelines.

Posterior fossa acute extradural hematoma is a rare but potentially fatal disease in children. This article reviews the literature on this topic and offers an evidence based guideline for management of the same.

INTRODUCTION

Children are susceptible to fall, and trauma to the back of the head is quite common among them. However, injury sufficient enough to cause a fracture of the occipital bone and produce acute extradural hematoma is quite rare—1.3% of all head injuries.[1] However, if there is an acute extradural hematoma accumulation in the posterior fossa, then the child can have a precipitous drop in the neurological status because of small volume of the posterior fossa and brain stem compression. The idea of this review is to produce evidence-based guideline of this rare but potentially lethal complication in children.

MATERIALS AND METHODS

A MEDLINE search involving keywords such as “posterior fossa,” “epidural,” or “extradural hematoma,” and “children” returned approximately 157 peer-reviewed articles between the years 1953 and 2017. A surge of publications was observed around the year 1990, presumably with the advent and widespread availability of computerized tomography (CT) scan machines worldwide. On further scrutiny, it was found that 41 articles actually dealt with pediatric acute posterior fossa extradural hematoma (PFEDH), and those were analyzed in this observation (Chart 1).

Chart 1

Pubmed Search – Keywords : Posterior fossa extradural hematoma, children. Number of articles yearwise

INCIDENCE

PFEDH is rare. It accounts for less than 0.13% to 1.9% of all traumatic head injuries.[23] The rarity is because of the early ossification and due thickness of the basioccipital bone, resulting in less amount of fracture as compared to supratentorial counterparts. PFEDH accounts for 4%–12.9% of all acute extradural hematoma cases.[1456] A gross disparity between the incidence in children and adults has been observed—one in three PFEDH cases occurs in children. The male:female ratio is also skewed in favor of boys who are 3.5 times more prone to develop PFEDH than girls.[7]

ETIOPATHOGENESIS

The majority of the PFEDH cases are traumatic. The various scenarios in the order of incidence are falls, road traffic accidents, and sporting activities.[14] The majority of the falls observed in children are domestic or at school. Most of the injuries are direct or coup injuries as the child falls backward on the occiput. A total of 78%–93% of the cases have occipital fractures that are mainly linear.[3] Mahapatra et al.,[4] in a retrospective analysis of 22 patients over 6 years, found that 73% had occipital fracture. Contrecoup injuries are observed in road traffic accidents and fall from greater heights. They usually have associated supratentorial and/or brain stem injuries. The incidence of PFEDH is more in children than in adults—23.3% versus 12.7% in Suyama series.[8] Children have the dura and venous sinuses as opposed to the bones, and bleeding from the venous sinus leads to progressive stripping of the dura from the bone and an expanding PFEDH. Rarely PFEDH is seen in association with other bleeding diathesis,[9101112] systemic illness,[13] after cardiac surgery,[14] and malignancies such as angiosarcoma,[15] presenting either spontaneously or after a fall.

SYMPTOMATOLOGY

PFEDH symptoms are initially subtle and are often missed in the pre-CT era. The child presents with occipital pain and headache and a few episodes of vomiting, which settle down with rest and analgesics. Pillay and Peter[16] concluded that in children, lucid interval is an exception rather than the rule. Only one patient in Hernesniemi series[17] had a classical lucid interval, whereas Krishnan[18] described late decompensation in a chronic case after a prolonged lucid interval. With the passage of time, drowsiness creeps in and the child becomes rapidly unresponsive because of brain stem compression and hydrocephalus. Ascending transtentorial “reverse herniation” gives rise to medullary pattern respiration and ensuing death. Once a critical volume of hematoma is reached, the deterioration occurs quite rapidly. In less severe cases, the child complains of persistent neck pain. Neck pain and partial torticollis are signs of impending tentorial herniation, which are not to be missed. Subacute cases show cerebellar signs. In cases of severe primary injury involving the brain stem, the child becomes unresponsive from the beginning, in which case, the clinical monitoring of an expanding PFEDH becomes all the more difficult.

DIAGNOSIS

The gold standard of diagnosis of a PFEDH is CT scan. The CT scan detects hematoma most early and reliably. Occipital linear fractures may be detected in almost 80% of the cases by CT scan. However, a possibility of missing a thin linear fracture in axial cut of CT scan must always be kept in mind in all pediatric trauma patients. Hyperacute CT scan also misses an enlarging PFEDH, and so the timing of the scan is also important. A delay of 4–6 h after a recognized fall can pick up most if not all of the PFEDH cases. The patients, in whom CT scan was already carried out early, will need a repeat CT scan after 6 h if there is a clinical suspicion.[19] In a large series of 14 patients, Gupta et al.[20] advocated the liberal use of CT scan. Specific note must be made about the volume of clot, distortion of fourth ventricle, posterior fossa cisterns, basal cisterns especially interpeduncular, and ambient and crural cistern effacement or obliteration. Mahapatra et al.[4] also noted that the mean volume of clot was almost three times higher in the operative group. Magnetic resonance imaging and magnetic resonance venogram are indicated in cases of suspected dural sinus injury, brain stem injury, or basal ganglion involvement. It may also detect early evidence of cerebral herniation. Approximately 50% of the patients had associated intradural lesions, and a similar incidence was also noted by Zuccarello et al.,[21] suggesting high-speed injuries are more common in the Western world. Coagulation profile is mandatory in all the cases as majority of the PFEDH cases will need surgical evacuation as discussed below.

MANAGEMENT

Management protocol will depend on the clinical condition of the patient at the time of admission. Glasgow Coma Scale (GCS) score assessments at presentation and follow-ups at regular intervals are mandatory. In a patient with GCS score of 15/15, repeated follow-ups with rest, analgesics, and serial scans are recommended. In a patient with falling GCS score, especially if it is below 12, urgent repeat CT scan is recommended. The largest series reported by Sencer et al.[19] had achieved excellent outcomes by triaging patients according to GCS scores and serial CT scan findings. Clot more than 10 mm in thickness, cisternal obliteration, fourth ventricle distortion, and brain stem compression are unequivocal indications of surgical removal. In those cases, where the CT scan is equivocal and/or the epidural has become subacute and chronic, expectant management can be continued with serial intermittent scans. Pang et al.[22] described a series of conservatively treated PFEDH cases and stressed the monitoring of subtle signs of brain dysfunction during the phase of clot expansion before clot resorption. In such cases, intracranial pressure monitoring and CT surveillance of hydrocephalus in neurosurgical intensive care unit with a low threshold for operation was helpful.[2324] However, surgery was the preferred treatment modality in almost all published series. Indications of surgery in Otsuka series were maximum clot thickness >1.5 cm, poor visualization of posterior fossa cisterns, marked deformity of the fourth ventricle, and supratentorial extension of the clot.[25] A management algorithm is given here as a guideline (Chart 2). Surgery involves carrying out a fast decompressive craniectomy of posterior fossa and evacuating the epidural clot. Intensive waxing of fractured bone segments must be carried out. Dural venous sinus bleeding is to be controlled by the pressure of patty made of oxidized cellulose wrapped over gelatin sponge. In torrential bleeding, sinus may be skeletonized and may require to be clipped by Ligaclip (Ethicon, Endosurgery, USA). Hemostatic matrix may also be used in desperate cases. Children have large occipital sinus, and torrential venous bleeding may be encountered in fractures crossing midline. However, most groups recommend surgery even if the children are asymptomatic because of the possibility of rapid deterioration versus performing a relatively safe prophylactic surgery.

Chart 2

Our proposed management guidelines for PFEDH: Legends: Rx – medical treatment, Sx- surgical evacuation

PROGNOSIS

If left untreated, PFEDH that is expanding has a very high mortality and morbidity rates. Hernesniemi et al.,[17] in a large series of 24 patients over 6 years, concluded that the best outcome is obtained in admission GCS scores of 14–15 and worst outcomes are seen in patients with associated intradural lesions. Respiratory arrest may signify irreversible decompensation and can herald death in spite of emergency evacuation.[26] Hydrocephalus is an ominous sign observed in CT scan.[27] Neurological observation by trained staff is an absolute necessity in such cases. Berker et al.[28] concluded that surgical evacuation gives the patient a chance of total recovery. However children have better outcomes than adults in most series.[2930] This is due to the fact that more frequently the bleed is venous than in adults and epidural hematomas in children tend to liquefy early than supratentorial hematomas.[31]

CONCLUSION

PFEDH is a potentially lethal disease observed particularly in children. Quick recognition and surgical evacuation is the key for good outcome. Surgery is the cornerstone of its treatment, and the timing of surgery is an essence.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.